溃结改良方改善DSS诱导的UC小鼠肠道炎症反应的机制研究
Effect of Kuijie Gailiang Prescription Regulating Treg/Th17 Balance on Intestinal Inflammatory Response in DSS Mice
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摘要: 目的 从效应T细胞活化的源头Treg、Th17细胞入手，探讨溃结改良方(Kuijie Gailiang Prescription，KGP)调节Th17和Treg细胞的平衡转化机制，揭示溃结改良方治疗溃疡性结肠炎（Ulcerative colitis，UC）的深层次作用机理及作用靶点。方法 采用3.5%DSS诱导复制UC小鼠模型，并随机分为正常组、模型组、5-ASA组和溃结改良方低、高剂量组，每组8只。观察各组小鼠体质量、大便黏稠度及出血情况，计算疾病活动指数；结肠组织HE染色，观察远端结肠组织病理形态学变化；流式细胞术检测小鼠脾脏淋巴细胞Treg、Th17细胞水平。结果 溃结改良方对UC小鼠具有治疗效应，其疾病活动指数明显降低（P＜0.05），结肠病理改变得到改善。与正常组相比，模型组CD4+CD25+Foxp3+Treg细胞、IL-10、Foxp3、Smad3下调，CD3+CD4+IL-17A+Th17细胞、IL-17A、RORγt、STAT3蛋白上调，差异具有统计学意义（P＜0.01）；溃结改良方治疗后，CD4+CD25+Foxp3+Treg细胞、IL-10、Foxp3、p-Smad3上调，CD3+CD4+IL-17A+Th17细胞、IL-17A、RORγt、p-STAT3下降，与模型组比较差异具有统计学意义（P＜0.01）。结论 溃结改良方可能通过调控UC小鼠Treg/Th17免疫平衡起到治疗UC的作用。Abstract: OBJECTIVE To investigate the mechanism of balance transformation of Th17 and Treg by Kuijie Gailiang Prescription (KGP) and to investigate the role of KGP in the treatment of ulcerative colitis (UC) from the source of effector T cell activation Treg and Th17 cells. Deep-level mechanism of action and targets. METHODS The UC mouse model was induced by 3.5% DSS and randomly divided into normal group， model group， 5-ASA group and low and high dose KGP group， with 8 rats in each group. Observe the body mass， stool consistency and hemorrhage of each group， calculate the index of disease activity， observe the pathological changes of colon tissue by HE staining of colon tissue， and detect the levels of Treg and Th17 cells in mouse spleen by flow cytometry. RESULTS KGP had a therapeutic effect on UC mice. The disease activity index was significantly reduced (P<0.05)， and the pathological changes of colon tissue were improved. Compared with the normal group， the levels of CD4+CD25+Foxp3+ Treg， IL-10， Foxp3， and Smad3 were down-regulated， and the levels of CD3+CD4+IL-17A+Th17， IL-17A， RORγt， and STAT3 were up-regulated in the model group (P<0.01); after KGP treatment， The levels of CD4+CD25+Foxp3+ Treg， IL-10， Foxp3， and p-Smad3 were up-regulated， and the levels of CD3+CD4+IL-17A+Th17， IL-17A， RORγt， and p-STAT3 were decreased. There was a statistically significant difference compared with the model group (P<0.01). CONCLUSION KGP may play a role in the treatment of UC by regulating Treg/Th17 immune balance in UC mice.
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Keywords:
- Kuijie Gailiang Prescription /
- ulcerative colitis /
- Treg /
- Th17
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